Affinage

EPOR

Erythropoietin receptor · UniProt P19235

Length
508 aa
Mass
55.1 kDa
Annotated
2026-06-09
100 papers in source corpus 30 papers cited in narrative 30 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

EPOR is the erythropoietin receptor, a cytokine receptor that converts EPO binding into a JAK2-driven signaling program controlling erythroid progenitor survival, proliferation, and differentiation (PMID:18239084, PMID:16407844). Upon stimulation, JAK2 phosphorylates EPOR cytoplasmic tyrosines that nucleate distinct effector arms: STAT5 activation is the critical downstream node for erythropoiesis, and constitutively active STAT5 alone rescues proliferation of both Jak2-/- and EpoR-/- cells, while Stat5-dependent induction of Bcl-XL prevents erythroblast apoptosis during terminal differentiation (PMID:18239084, PMID:16407844). EPOR also drives Shc-independent Raf1/MEK/ERK activation via Shp2/Grb2 and a PI3K arm required for progenitor renewal (PMID:8978277, PMID:11439328). Phosphorylated Y429/Y431/Y479 recruit the p85 subunit of PI3K, which—after Cbl-dependent ubiquitination and engagement of epsin-1—drives clathrin-mediated endocytosis that terminates signaling; C-terminal truncating mutations underlying primary familial and congenital polycythemia (PFCP) abolish p85 binding and internalization, causing EPO hypersensitivity and persistent receptor activation (PMID:19336760, PMID:24113870, PMID:24533580, PMID:22253704). Signal magnitude is further constrained by a layered negative-feedback network including STAT5-induced SOCS/CIS proteins and Sprouty/Spred regulators that dampen JAK2 and ERK (PMID:12396724, PMID:28038963, PMID:22508938, PMID:22808010). Beyond erythropoiesis, EpoR is functionally expressed and signals through the same axis in osteoprogenitors and the monocytic lineage to regulate bone homeostasis (PMID:34518518, PMID:36233351), in white adipose tissue via an EpoR-RUNX1 axis controlling energy metabolism (PMID:39284834), and in macrophages where surface receptor levels gate M2 polarization (PMID:34925338).

Mechanistic history

Synthesis pass · year-by-year structured walk · 21 steps
  1. 1993 Medium

    Defining the EPO-binding region of the receptor established which extracellular epitopes mediate ligand engagement and could neutralize signaling.

    Evidence Monoclonal antibodies against the human EpoR extracellular domain tested in EPO competition binding and growth-inhibition assays

    PMID:7686789

    Open questions at the time
    • No atomic structure of the EPO-EPOR complex resolved here
    • Does not address intracellular signal transduction
  2. 1993 Medium

    Identifying a complex between SFFV gp52 env and EpoR showed the receptor can be aberrantly engaged, but processing—not mere binding—drives pathogenic mitogenesis.

    Evidence Co-immunoprecipitation of gp52 with EpoR plus glycosylation mutants in mitogenicity and splenomegaly assays

    PMID:8437218

    Open questions at the time
    • Mechanism of how processed gp52 activates EpoR not defined
    • Relevance to physiological EPO signaling limited
  3. 1997 Medium

    EPO was shown to activate Raf1/ERK through Shp2/Grb2 rather than Shc, distinguishing the EpoR MAPK arm from other cytokine receptors.

    Evidence EPO/IL-2/IL-15 stimulation of CTLL-EPO-R cells with Shc/Shp2 immunoprecipitation and Raf1/ERK2 kinase assays

    PMID:8978277

    Open questions at the time
    • Receptor tyrosines responsible for Shp2/Grb2 recruitment not mapped here
    • Single-lab biochemistry
  4. 1998 High

    Replacing EpoR with the prolactin receptor in EpoR-/- progenitors established that EpoR provides a permissive, not instructive, signal for erythroid differentiation.

    Evidence Retroviral PrlR and PrlR/EpoR chimera transduction into EpoR-/- progenitors with prolactin/SCF differentiation assays

    PMID:9716574

    Open questions at the time
    • Does not exclude EpoR-specific roles in non-erythroid tissues
    • Quantitative signaling differences not measured
  5. 1999 Medium

    A truncated EPOR isoform acting as a dominant negative linked aberrant receptor forms to ineffective erythropoiesis in disease.

    Evidence Stable EPOR-T transfection in UT-7/GM cells with apoptosis/hemoglobinization assays and RT-PCR in MDS patient samples

    PMID:10029161

    Open questions at the time
    • Causal role of EPOR-T in MDS pathogenesis not established
    • Mechanism of dominant-negative interference not detailed
  6. 2001 High

    Genetic and developmental studies placed EpoR signaling as both essential for progenitor renewal via PI3K and sufficient to advance the developmental switch to definitive erythropoiesis.

    Evidence p53-/- erythroid progenitor lines with STAT5/PI3K inhibition, and a constitutively active EpoR-R129C knock-in mouse

    PMID:11439328 PMID:11520789

    Open questions at the time
    • Downstream PI3K effectors for renewal not defined
    • How R129C accelerates the developmental switch mechanistically unclear
  7. 2002 Medium

    Mapping SOCS/CIS induction to STAT5 established the negative-feedback layer that limits EPOR proliferative signaling.

    Evidence STAT5/MAPK/PI3K inhibition, EpoR mutant lines activating signaling subsets, and inducible SOCS overexpression with reporter assays

    PMID:12396724

    Open questions at the time
    • Receptor docking sites for individual SOCS proteins not all mapped
    • Relative in vivo contribution of each SOCS not addressed
  8. 2003 Medium

    Two studies refined the EPOR cytoplasmic survival code—SLAP as a STAT5-inhibiting negative regulator and a tyrosine-independent membrane-proximal STAT5 survival signal.

    Evidence SLAP-EpoR co-IP and overexpression in erythroblasts; tyrosine-null EPOR mutants with dominant-negative STAT5 in 32D cells

    PMID:12946994 PMID:14662339

    Open questions at the time
    • How non-tyrosine sequences couple to STAT5 unresolved
    • SLAP interaction surface on EpoR not mapped
  9. 2006 High

    Genetic dissection established cell-autonomous requirements for EpoR, STAT5, and GR in erythroblast renewal and pinned terminal-differentiation survival on STAT5-driven Bcl-XL.

    Evidence Primary erythroblasts from EpoR-H, GRdim, and Stat5ab-/- mice with retroviral Bcl-XL rescue

    PMID:16407844

    Open questions at the time
    • Integration of GR with EpoR/STAT5 signaling not molecularly defined
    • Targets beyond Bcl-XL not enumerated
  10. 2008 Medium

    EPOR signaling was extended beyond the marrow to hepatic iron regulation via C/EBPalpha-dependent hepcidin suppression, and to KIT co-signaling through Y343.

    Evidence Anti-EPOR blocking antibody and C/EBPalpha ChIP in hepatocytes; KIT/EpoR tyrosine-to-phenylalanine mutants in 32D proliferation assays

    PMID:18326822 PMID:18538998

    Open questions at the time
    • Direct transcriptional mechanism linking EpoR to C/EBPalpha not resolved
    • In vivo relevance of KIT-EpoR Y343 cooperativity not tested genetically
  11. 2008 High

    Constitutively active STAT5 rescuing both Jak2-/- and EpoR-/- erythroid cells placed STAT5 as the critical effector node downstream of the receptor.

    Evidence Genetic rescue with cS5 in KO fetal liver cells, tamoxifen-inducible Stat5a-ER, and fetal liver transplantation

    PMID:18239084

    Open questions at the time
    • Full STAT5 target program not defined here
    • Roles of parallel PI3K/ERK arms not separated
  12. 2009 High

    Defining clathrin-mediated EPOR endocytosis via JAK2, Y429/Y431/Y479, and p85 recruitment established the signal-termination machinery and its failure in PFCP.

    Evidence EpoR tyrosine mutagenesis, p85alpha/beta knockdown and dominant negatives, clathrin inhibition, and PFCP mutant analysis

    PMID:19336760

    Open questions at the time
    • p85's PI3K-independent endocytic adaptor mechanism not fully detailed
    • Kinetics of receptor recycling vs. degradation not resolved
  13. 2012 High

    Multiple studies clarified EPOR trafficking, the molecular forms of the receptor, transcriptome targets, Spry1-mediated feedback, EpoR-independent JAK2V617F adhesion signaling, and EpoR control of red cell size.

    Evidence Domain-specific antibodies with N-glycanase/BFA; CFU-e transcriptome with Tnfr-sf13c validation; Mx1-Cre Spry1 deletion with LC-MS/MS PY53 discovery; EpoR knockdown in HEL cells; EpoR-/- and in vivo MCV measurements

    PMID:22253704 PMID:22508938 PMID:22808010 PMID:23160466 PMID:34921133

    Open questions at the time
    • Mechanism coupling EpoR to MCV control not molecularly defined
    • Spry1 target (Jak2 vs ERK) directness not fully separated
  14. 2013 High

    Cbl-dependent p85 ubiquitination engaging epsin-1 completed the endocytic mechanism and explained PFCP Epo hypersensitivity via lost negative feedback.

    Evidence Cbl knockdown/dominant negatives, epsin-1 UIM mutants, co-localization, and rescue of p85-binding in PFCP receptors

    PMID:24113870

    Open questions at the time
    • E3 ligase specificity for p85 vs receptor not fully resolved
    • In vivo contribution to polycythemia not genetically tested here
  15. 2014 Medium

    Chimeric-receptor analysis of PFCP mutants mechanistically linked C-terminal truncation to slower degradation, mature glycoforms, and extended signaling.

    Evidence EGFR-EPOR chimeras carrying PFCP deletions/nonsense/missense alleles with glycosylation, degradation, and signaling-duration readouts

    PMID:24533580

    Open questions at the time
    • Chimeric system may not fully mimic native EPOR
    • Quantitative contribution of each mutation to disease severity unknown
  16. 2016 Medium

    Mapping CIS to phospho-Y401 connected a specific receptor docking site to STAT5/ERK control and tumor suppression in JAK2V617F cells.

    Evidence CIS-EpoR co-IP at Y401, CIS RNAi/overexpression with SH2 mutants, STAT5/ERK assays, and nude mouse tumor formation

    PMID:28038963

    Open questions at the time
    • Direct vs indirect Y401-CIS binding not structurally confirmed
    • In vivo erythroid relevance of CIS-Y401 not tested
  17. 2020 Medium

    PTPN18 was identified as a JAK2-dependent EPO target phosphatase that sustains EPOR signaling and modulates receptor glycoforms and RHEX phosphorylation.

    Evidence Phospho-tyrosine PTM proteomics, PTPN18-Y389 mutagenesis, JAK2 inhibition, RHEX phospho-assays, and proliferation/survival readouts

    PMID:32027948

    Open questions at the time
    • Direct PTPN18 substrates not all defined
    • In vivo erythroid role of PTPN18 untested
  18. 2021 High

    Tissue-specific genetics and reporters revealed EpoR function and expression beyond erythroid cells—in osteoprogenitors regulating bone, in EBI macrophages and diverse hematopoietic subsets, and a Rab26-dependent surface-trafficking requirement for macrophage M2 polarization.

    Evidence EpoR:Osx-cre cKO with histomorphometry and osteoclast co-culture; EpoR-tdTomato-Cre reporter with EPO injection; myeloid EPOR-deficient and Rab26-KO macrophages with eCIRP and polarization assays

    PMID:34098576 PMID:34518518 PMID:34925338

    Open questions at the time
    • Whether non-erythroid EpoR uses identical JAK2/STAT5 wiring not fully established
    • Physiological ligand levels driving non-erythroid signaling unclear
  19. 2022 Medium

    Monocytic-lineage EPOR deletion showed EpoR signaling in osteoclast precursors mediates EPO-induced bone loss independently of erythropoiesis.

    Evidence LysMCre and Cx3cr1Cre EPOR cKO mice with EPO challenge, CD115+ preosteoclast flow cytometry, and microCT

    PMID:36233351

    Open questions at the time
    • Downstream effectors in osteoclast precursors not mapped
    • Sex-specific effects not mechanistically explained
  20. 2023 High

    EpoR-driven JAK2 phosphorylation of p27Kip1 at Y88 was shown to convert p27 from CDK inhibitor to activator, providing a proliferative mechanism with an in vivo erythroid phenotype.

    Evidence p27-EpoR co-IP, Y88 phosphorylation with JAK2 inhibitor, p27Y88F knock-in mice, and CFU-E/CBC analysis

    PMID:37443738

    Open questions at the time
    • Whether p27Y88 phosphorylation is direct by JAK2 not fully resolved
    • Contribution relative to STAT5-driven proliferation unquantified
  21. 2024 High

    An EPO-EpoR-RUNX1 axis in white adipose tissue was defined, where EPO stabilizes RUNX1 by lowering FBXW7 to suppress lipogenesis and control energy metabolism.

    Evidence Adipose-specific EpoR-KO mice with EPO treatment, RUNX1 stability and FBXW7 expression assays, and lipogenic gene profiling

    PMID:39284834

    Open questions at the time
    • Signaling steps from EpoR to FBXW7 regulation not defined
    • Sex-specific (male) phenotype mechanism unexplained

Open questions

Synthesis pass · forward-looking unresolved questions
  • Whether non-erythroid EpoR functions (bone, adipose, macrophage) employ the same JAK2/STAT5/PI3K/ERK wiring and receptor tyrosines as erythroid signaling remains unresolved.
  • No tissue-by-tissue mapping of EpoR tyrosine usage
  • Endogenous ligand and dosage driving non-erythroid signaling unclear
  • No structural model of full-length receptor signaling complexes in the corpus

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 3 GO:0098772 molecular function regulator activity 3 GO:0048018 receptor ligand activity 2
Localization
GO:0005886 plasma membrane 3 GO:0031410 cytoplasmic vesicle 3 GO:0005783 endoplasmic reticulum 2
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3 R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-1266738 Developmental Biology 2

Evidence

Reading pass · 30 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 Epo-induced endocytosis of EpoR occurs via clathrin-mediated endocytosis. Both JAK2 kinase activity and EpoR cytoplasmic tyrosines (Y429, Y431, Y479) are required for ligand-dependent EpoR internalization. Phosphorylated Y429, Y431, and Y479 bind the p85 subunit of PI3K upon Epo stimulation, and p85α/β recruit endocytic machinery in a PI3K activity-independent manner. Truncated EpoRs from PFCP patients lacking these tyrosines fail to bind p85 or internalize upon stimulation. Mutagenesis of EpoR cytoplasmic tyrosines, knockdown of p85α/p85β with dominant-negative constructs, clathrin inhibition assays, analysis of PFCP patient receptor mutants Blood High 19336760
2013 Epo induces Cbl-dependent ubiquitination of the p85 regulatory subunit of PI3K, which is bound to phosphotyrosines on EpoR. Ubiquitinated p85 interacts with endocytic protein epsin-1, driving EpoR endocytosis. Knockdown of Cbl or expression of epsin-1 mutants lacking ubiquitin-interacting motifs impairs EpoR internalization. PFCP-mimicking EpoR mutants cannot bind p85, co-localize with epsin-1, or internalize, causing Epo hypersensitivity. Restoring p85 binding to PFCP receptors rescues epsin-1 co-localization and EpoR internalization. Cbl knockdown, dominant-negative Cbl expression, epsin-1 UIM mutants, co-localization assays, primary erythroid progenitor knockdown, rescue experiments with restored p85-binding EpoR Blood High 24113870
2008 EPO regulates hepcidin expression in a dose-dependent manner in hepatocytes through EPOR signaling. This is mediated through the transcription factor C/EBPα: EPO treatment decreases C/EBPα binding to the hepcidin promoter, as shown by chromatin immunoprecipitation. Pre-treatment with an EPOR-blocking antibody restores hepcidin mRNA levels, confirming EPOR dependence. Anti-EPOR blocking antibody, chromatin immunoprecipitation (ChIP) for C/EBPα at the hepcidin promoter, RT-PCR/Western blot for C/EBPα, freshly isolated mouse hepatocytes and HepG2 cells Blood Medium 18326822
2008 Constitutively activated Stat5a (cS5) is sufficient to rescue erythroid proliferation in both Jak2−/− and EpoR−/− cells in an Epo-independent manner, and tamoxifen-induced DNA binding of a Stat5a-ER fusion construct enables erythropoiesis in the absence of Epo. This places activated Stat5 as a critical downstream effector of Jak2 in erythropoiesis, functionally downstream of EpoR. Genetic rescue with constitutively active Stat5a mutant in Jak2−/− and EpoR−/− fetal liver cells, tamoxifen-inducible Stat5a-ER construct, fetal liver transplantation into irradiated mice Blood High 18239084
2001 Stat5 and PI3K signaling pathways are utilized by both EpoR/c-Kit and v/c-ErbB in erythroid progenitor expansion. v-ErbB-transformed cells and normal progenitors depend on PI3K signaling for renewal, establishing that EpoR-driven PI3K signaling is essential for erythroid progenitor renewal. Immortalized erythroid progenitor lines from p53−/− fetal livers, ErbB inhibition, inhibition of Stat5 and PI3K, comparison with EpoR/c-Kit–driven expansion Oncogene Medium 11439328
2001 EpoR expression and activation regulate the timing of the definitive wave of erythropoiesis. A constitutively active form of EpoR (R129C EpoR) knocked into mice leads to earlier onset of definitive erythropoiesis in the yolk sac, demonstrating that EpoR signaling activation is sufficient to advance the developmental switch between primitive and definitive erythropoiesis. Knock-in mouse model with constitutively active EpoR-R129C, spatial/temporal analysis of Epo and EpoR gene expression during embryogenesis Blood High 11520789
1998 The prolactin receptor (PrlR) can fully replace EpoR in supporting terminal differentiation of EpoR−/− erythroid progenitors, demonstrating that EpoR has no instructive or unique signaling role in red blood cell differentiation beyond generic cytokine receptor signaling. Additionally, the synergistic interaction between EpoR and c-Kit is fully reproduced by PrlR and c-Kit, showing no requirement for an EpoR-unique signal in this synergism. Retroviral transduction of PrlR and PrlR/EpoR chimera into EpoR−/− progenitors, in vitro differentiation assays with prolactin and stem cell factor Blood High 9716574
1997 EPO activates the Raf1/MEK/MAP kinase pathway independently of Shc phosphorylation in CTLL-EPO-R cells. While IL-2 and IL-15 stimulate Shc tyrosine phosphorylation, EPO does not activate Shc but instead activates Raf1 and ERK2 through Shp2/Grb2/receptor complexes, establishing an Shc-independent Raf1 activation pathway downstream of EpoR. Stimulation of CTLL-EPO-R cells with EPO/IL-2/IL-15, immunoprecipitation of Shc and Shp2, Raf1 kinase assay, ERK2 kinase assay Blood Medium 8978277
2002 SOCS1, SOCS2, SOCS3, and CIS induction by EPO depends on Stat5 but not on MAPK or PI3K. SOCS1, SOCS3, and CIS overexpression negatively regulate EPO-mediated cell proliferation and Stat5 phosphorylation; SOCS2 is less effective; SOCS4 is ineffective. These results establish differential roles of SOCS family members downstream of EPOR signaling. Inhibition of specific signaling molecules (Stat5, MAPK, PI3K), EpoR mutant cell lines activating only subsets of signaling cascades, stable inducible SOCS overexpression cell lines, luciferase reporter assays Journal of interferon & cytokine research Medium 12396724
2006 Functional EpoR, Stat5, and glucocorticoid receptor (GR) are each cell-autonomously required for erythroblast renewal in vitro. Cells from EpoR-H mutant mice show enhanced differentiation instead of renewal. Additionally, Stat5ab is required for Epo-induced terminal differentiation: Stat5ab−/− differentiating erythroblasts undergo apoptosis due to absent Bcl-XL induction, a defect fully rescued by exogenous Bcl-XL. Primary erythroblast cultures from EpoRH, GRdim/dim, and Stat5ab−/− mice; retroviral Bcl-XL rescue; proliferation and differentiation assays Oncogene High 16407844
2003 SLAP (Src-like adaptor protein) forms a specific complex with EpoR in FLI-1-transformed erythroblasts. Constitutive SLAP expression severely impairs Epo-induced erythroid differentiation by inhibiting STAT5 activation and Bcl-X gene upregulation downstream of EpoR, establishing SLAP as a negative regulator of EpoR signaling. Co-immunoprecipitation of SLAP with EpoR, stable SLAP expression in primary erythroblasts, STAT5 phosphorylation assays, hemoglobinization assays Blood Medium 12946994
2012 EpoR signaling increases red cell size (MCV) while also increasing the number and speed of erythroblast cell cycles. EpoR-regulation of cell size is independent of iron-based size regulation. High EPO increases MCV in wild-type mice and human volunteers, and this effect outlasts EPO treatment duration. EpoR−/− erythroblasts with survival rescue signaling, comparison of cycling parameters, EPO injection in wild-type mice and human volunteers, MCV measurements Nature communications High 34921133
2012 JAK2V617F activates Lu/BCAM-mediated red cell adhesion through an EpoR-independent Rap1/Akt signaling pathway. Knockdown of EpoR in HEL cells does not alter Akt activity or cell adhesion to laminin, establishing that this JAK2V617F-driven pathway is distinct from EpoR. EpoR knockdown in HEL cells, dominant-negative Rap1S17N expression, Rap1 inhibitor GGTI-298, phospho-Akt measurement, laminin adhesion assays Blood Medium 23160466
2012 EPOR-regulated transcriptome analysis in primary CFU-e progenitors identified 160 EPO/EPOR target transcripts. SOCS2, Socs3, Spred1, Spred2, and Eaf1 serve as negative-feedback components. The atypical TNF-receptor Tnfr-sf13c is upregulated >5-fold by EPO via EPOR/Jak2/Stat5 and promotes proerythroblast survival and erythroblast formation. Global transcriptome analysis of primary bone marrow CFU-e progenitors, Tnfr-sf13c ligation survival assays, identification of EPOR/Jak2/Stat5 response genes PloS one Medium 22808010
2012 Spry1 is selectively expressed in CFU-e to erythroblast stages and is phosphorylated at its conserved PY53 motif by EpoR signaling upon EPO stimulation (discovered by LC-MS/MS). Conditional Spry1 deletion leads to hyperactivation of Erk1/2 and Jak2 in erythroid progenitors, identifying Spry1 as a negative feedback regulator and candidate suppressor of Jak2 downstream of EpoR. Mx1-Cre conditional Spry1 deletion, LC-MS/MS phosphoproteomic discovery of Spry1-PY53, signaling analysis in Spry1-null progenitors, anemia challenge models Blood High 22508938
2020 PTPN18, identified by phospho-tyrosine PTM proteomics as a novel EPO target (phosphorylated at Y389 in a JAK2-dependent manner), promotes EPO-dependent hematopoietic cell proliferation and survival. PTPN18 sustains EPO-induced activation of ERK1/2, AKT, STAT5, and JAK2. It also increases high-molecular-weight EPOR forms while inhibiting EPO-induced phosphorylation of the EPOR-associated adaptor RHEX at Y141. Each effect depends on PTPN18-Y389. Phospho-tyrosine PTM proteomics, ectopic PTPN18 expression, JAK2 inhibitor treatment, RHEX phosphorylation assays, cell proliferation/survival assays, EPOR molecular weight analysis Cellular signalling Medium 32027948
2016 CIS interacts with phosphorylated EpoR at Y401, which is critical for STAT5 and ERK activation. The SH2 domain and tyrosine phosphorylation of CIS at Y253 are required for its tumor-suppressive anti-proliferative effects in JAK2V617F-transformed cells. CIS knockdown enhances STAT5 and ERK activation in JAK2V617F cells; CIS overexpression suppresses these signals and inhibits tumor formation. CIS-EpoR co-immunoprecipitation at Y401, CIS RNA interference, CIS overexpression with SH2 domain mutants, STAT5/ERK phosphorylation assays, nude mouse tumor formation assay Cellular signalling Medium 28038963
2003 Non-tyrosine-containing sequences in the membrane-proximal region of EPOR elicit an important Stat5-dependent cell survival signal in 32D cells, independently of EpoR cytoplasmic tyrosines. This survival signal is serum-independent, revealing a previously unrecognized Stat5-dependent survival pathway in the EPOR cytoplasmic region. Stable transfection of 32D cells with wild-type and tyrosine-null EPOR mutants, dominant-inhibitory Stat5 isoform expression, EPO-dependent survival and proliferation assays Experimental hematology Medium 14662339
2008 KIT-associated intracellular tyrosines, particularly those binding Src kinases, are required for EpoR co-signaling. EpoR-Y343 is the single most important EpoR tyrosine for proliferation cooperativity with KIT, inducing Stat5, PI3K/Akt, and Erk1/2 activation. Restoration of the PLC-γ binding site in KIT antagonizes co-signaling with EpoR, while the Src binding sites are sufficient for restoring KIT–EpoR co-signaling. Co-expression of KIT and EpoR tyrosine-to-phenylalanine mutants in 32D cells, proliferation assays, STAT5/Akt/ERK phosphorylation analysis Cellular signalling Medium 18538998
2014 PFCP-associated EPOR mutations (deletion Del1377-1411, nonsense C1370A, missense G1445A) cause slower receptor degradation, higher levels of glycan-mature receptor forms, increased sensitivity to low ligand concentrations, and extended downstream signaling cascades, as studied using EGFR–EPOR chimeric receptors. These mechanisms explain Epo hypersensitivity in PFCP patients. EGFR–EPOR chimeric receptor system activated by EGF binding, Western blot for receptor glycosylation/degradation, signaling duration assays British journal of haematology Medium 24533580
2021 EpoR in osteoprogenitor cells (EpoR:Osx-cre conditional knockout) is required for normal bone homeostasis and for EPO-induced bone loss. Deletion of EpoR in osteoprogenitors reduced the RANKL/OPG ratio, decreased osteoblast-supported osteoclastogenesis, and protected female mice from EPO-induced trabecular bone loss and increased osteoclast numbers. This demonstrates that EpoR in osteoprogenitors regulates osteoblast function and osteoblast-mediated osteoclastogenesis. EpoR:Osx-cre conditional knockout mice, histomorphometry, serum bone markers (P1NP, osteocalcin, TRAP), osteoblast/osteoclast co-culture from cKO vs. control, EPO pump implantation Bone research High 34518518
1993 SFFV gp52 env protein forms an immunoprecipitable complex with EpoR in the endoplasmic reticulum. However, formation of this ER complex is not sufficient for either mitogenicity in cell culture or pathogenicity in mice; instead, processing of gp52 to more highly glycosylated forms is required for EpoR-dependent mitogenicity and splenomegaly. Glycosylation site mutants of SFFV env, co-immunoprecipitation of gp52 with EpoR, BaF3-epoR cell mitogenicity assays, mouse splenomegaly model Journal of virology Medium 8437218
1993 Six monoclonal antibodies (MoAbs) to the extracellular domain of human EpoR were generated. Four neutralizing (Group I) MoAbs compete with radiolabeled EPO for EpoR binding and inhibit EPO-dependent cell growth, identifying the EPO-binding epitope region. Two non-neutralizing MoAbs recognize discrete epitopes that do not overlap the EPO-binding site. Monoclonal antibody generation, immunoprecipitation of 35S-labeled EpoR, radiolabeled EPO competition binding assay, EPO-dependent Ba/F3-hEPO-R growth inhibition Blood Medium 7686789
2012 EPOR undergoes sharply ligand-dependent inward trafficking in UT7epo cells and primary proerythroblasts. EPOR-68K is a core-glycosylated intracellular pool and EPOR-70K comprises the apparent cell-surface EPOR population. Polycythemia-associated C-terminal truncated EPOR-T alleles are persistently activated upon EPO challenge, become over-represented during exponential growth, and result in EPO dose-dependent loss of endogenous wild-type EPOR through squelching of C-terminal-mediated negative feedback. Novel rabbit monoclonal antibodies to intracellular, phospho-activated, and extracellular EPOR domains; Brefeldin A treatment; N-glycanase digestion; Western blot analysis of EPOR forms; UT7epo and primary proerythroblast trafficking assays; expression of PFCP EPOR-T mutants PloS one Medium 22253704
2021 EpoR is expressed in erythroblastic island (EBI) macrophages (defined by tdTomato reporter in EpoR-tdTomato-Cre mice), as well as in subsets of hematopoietic stem cells, progenitors, megakaryocytes, B cells, spleen red pulp macrophages, and liver Kupffer cells. EPO injection selectively promotes proliferation of EpoR-expressing cells and induces erythroid lineage bias in hematopoiesis. EpoR-tdTomato-Cre knock-in reporter mouse, Cre-mediated floxed STOP excision validation, flow cytometry, EPO injection experiments Blood High 34098576
2022 EpoR signaling in the monocytic/osteoclast lineage contributes to EPO-induced bone loss. Conditional deletion of EPOR in the monocytic lineage using LysMCre significantly reduced the high-dose EPO-induced increase in bone marrow preosteoclasts (CD115+) and the resulting trabecular bone loss in female mice, without interfering with erythropoiesis. LysMCre EPOR conditional knockout mice, Cx3cr1Cre EPOR conditional knockout mice, high- and low-dose EPO administration, flow cytometry for CD115+ preosteoclasts, microCT bone volume measurements International journal of molecular sciences Medium 36233351
2023 EpoR activation leads to immediate Jak2-dependent phosphorylation of the CDK inhibitor p27Kip1 at tyrosine 88 (Y88), converting it from a CDK inhibitor to an activator/assembly factor of CDK4/6, thereby promoting erythroid progenitor proliferation. Knock-in mice with p27Y88F mutation exhibit lower red blood cell counts, lower hematocrit, and reduced CFU-E colony outgrowth. Co-immunoprecipitation of p27 with EpoR, p27-Y88 phosphorylation assays in presence of Jak2 inhibitor, p27Y88F knock-in mice, CFU-E colony assays, complete blood count analysis Cells High 37443738
2024 EPO regulates energy metabolism through the EPO-EpoR-RUNX1 axis. EpoR in white adipose tissue mediates metabolic activity; male mice with adipose-specific EpoR ablation show increased fat mass and obesity susceptibility. EPO treatment increases RUNX1 protein in adipose tissue by decreasing FBXW7 ubiquitin ligase expression, thereby stabilizing RUNX1, which directly inhibits lipogenic gene expression. This effect is absent in adipose-specific EpoR knockout mice. Adipose-specific EpoR knockout mice, EPO treatment of wild-type vs. knockout mice, RUNX1 protein stability assays, FBXW7 expression analysis, lipogenic gene expression profiling Nature communications High 39284834
1999 A truncated form of human EPO receptor (EPOR-T) acts as a dominant negative regulator of EPO-induced erythroid differentiation. EPOR-T transfection in UT-7/GM cells induces apoptosis in the presence of EPO and blocks EPO-induced erythroid differentiation and hemoglobinization. EPOR-T is expressed in 7/9 myelodysplastic syndrome cases but not in normal controls, suggesting it may contribute to ineffective erythropoiesis in MDS. Stable transfection of EPOR-T in UT-7/GM cells, EPO-dependent hemoglobinization assay, apoptosis assay, RT-PCR in MDS patient samples Experimental hematology Medium 10029161
2021 Extracellular CIRP (eCIRP) reduces macrophage surface EPOR levels by impairing Rab26, a member of the Ras family of small G proteins that controls EPOR transport to the cell surface. Impaired Rab26 reduces surface EPOR, which restrains EPOR-mediated M2 macrophage polarization. EPO treatment fails to promote M2 polarization in Rab26 knockout macrophages, establishing Rab26 as required for EPOR surface expression and downstream macrophage polarization signaling. Myeloid-specific EPOR-deficient mice, Rab26 knockout macrophages, eCIRP treatment, flow cytometry for surface EPOR, macrophage polarization assays, LPS-induced ALI model Frontiers in immunology Medium 34925338

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 Erythropoietin mediates hepcidin expression in hepatocytes through EPOR signaling and regulation of C/EBPalpha. Blood 188 18326822
2001 Leukemic transformation of normal murine erythroid progenitors: v- and c-ErbB act through signaling pathways activated by the EpoR and c-Kit in stress erythropoiesis. Oncogene 86 11439328
2008 Stat5 activation enables erythropoiesis in the absence of EpoR and Jak2. Blood 85 18239084
2010 Absence of functional EpoR expression in human tumor cell lines. Blood 83 20124514
2012 JAK2V617F activates Lu/BCAM-mediated red cell adhesion in polycythemia vera through an EpoR-independent Rap1/Akt pathway. Blood 78 23160466
2020 Suppression of NLRP3 Inflammasome by Erythropoietin via the EPOR/JAK2/STAT3 Pathway Contributes to Attenuation of Acute Lung Injury in Mice. Frontiers in pharmacology 72 32265704
2017 Erythropoietin ameliorates early brain injury after subarachnoid haemorrhage by modulating microglia polarization via the EPOR/JAK2-STAT3 pathway. Experimental cell research 66 29102603
2009 Identification of a sensitive anti-erythropoietin receptor monoclonal antibody allows detection of low levels of EpoR in cells. Journal of immunological methods 57 19887071
2001 Erythropoietin (Epo) and EpoR expression and 2 waves of erythropoiesis. Blood 57 11520789
1998 The prolactin receptor rescues EpoR-/- erythroid progenitors and replaces EpoR in a synergistic interaction with c-kit. Blood 53 9716574
2009 Ligand-induced EpoR internalization is mediated by JAK2 and p85 and is impaired by mutations responsible for primary familial and congenital polycythemia. Blood 47 19336760
2021 EpoR stimulates rapid cycling and larger red cells during mouse and human erythropoiesis. Nature communications 46 34921133
2006 Erythroid progenitor renewal versus differentiation: genetic evidence for cell autonomous, essential functions of EpoR, Stat5 and the GR. Oncogene 46 16407844
1997 Erythropoietin activates Raf1 by an Shc-independent pathway in CTLL-EPO-R cells. Blood 43 8978277
2002 Differential roles of SOCS family members in EpoR signal transduction. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 41 12396724
2017 Erythropoietin Rescues Memory Impairment in a Rat Model of Chronic Cerebral Hypoperfusion via the EPO-R/JAK2/STAT5/PI3K/Akt/GSK-3β Pathway. Molecular neurobiology 36 28488208
2021 EpoR-tdTomato-Cre mice enable identification of EpoR expression in subsets of tissue macrophages and hematopoietic cells. Blood 35 34098576
2017 Neuroprotective effects of erythropoietin against sevoflurane-induced neuronal apoptosis in primary rat cortical neurons involving the EPOR-Erk1/2-Nrf2/Bach1 signal pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 35 28064106
1990 Assignment of the erythropoietin receptor (EPOR) gene to mouse chromosome 9 and human chromosome 19. Genomics 35 1962754
2013 Cbl ubiquitination of p85 is essential for Epo-induced EpoR endocytosis. Blood 32 24113870
1995 Lineage-restricted recruitment of immature hematopoietic progenitor cells in response to Epo after normal hematopoietic cell transfection with EpoR. Experimental hematology 32 7601257
2019 Venlafaxine Mitigates Depressive-Like Behavior in Ovariectomized Rats by Activating the EPO/EPOR/JAK2 Signaling Pathway and Increasing the Serum Estradiol Level. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics 31 30361931
2016 Erythropoietin accelerates tumor growth through increase of erythropoietin receptor (EpoR) as well as by the stimulation of angiogenesis in DLD-1 and Ht-29 xenografts. Molecular and cellular biochemistry 29 27543111
2008 Synergistic upregulation of erythropoietin receptor (EPO-R) expression by sense and antisense EPO-R transcripts in the canine lung. Proceedings of the National Academy of Sciences of the United States of America 28 18495932
2017 Expansion of EPOR-negative macrophages besides erythroblasts by elevated EPOR signaling in erythrocytosis mouse models. Haematologica 27 29051279
2016 Erythropoietin attenuates renal and pulmonary injury in polymicrobial induced-sepsis through EPO-R, VEGF and VEGF-R2 modulation. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 27 27470403
2021 Epo/EpoR signaling in osteoprogenitor cells is essential for bone homeostasis and Epo-induced bone loss. Bone research 26 34518518
2017 Erythropoietin drives breast cancer progression by activation of its receptor EPOR. Oncotarget 26 28418910
2016 Expression of multidrug resistance protein P-glycoprotein in correlation with markers of hypoxia (HIF-1α, EPO, EPO-R) in invasive breast cancer with metastasis to lymph nodes. Archives of medical science : AMS 26 29181060
2014 Ginsenoside Rg1 induces apoptosis through inhibition of the EpoR-mediated JAK2/STAT5 signalling pathway in the TF-1/ Epo human leukemia cell line. Asian Pacific journal of cancer prevention : APJCP 26 24761846
2010 Testosterone membrane-initiated action in breast cancer cells: Interaction with the androgen signaling pathway and EPOR. Molecular oncology 25 20189893
2021 Extracellular CIRP-Impaired Rab26 Restrains EPOR-Mediated Macrophage Polarization in Acute Lung Injury. Frontiers in immunology 23 34925338
2011 Different expression patterns of Ngb and EPOR in the cerebral cortex and hippocampus revealed distinctive therapeutic effects of intranasal delivery of Neuro-EPO for ischemic insults to the gerbil brain. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 23 21339183
1999 Dominant negative effect of a truncated erythropoietin receptor (EPOR-T) on erythropoietin-induced erythroid differentiation: possible involvement of EPOR-T in ineffective erythropoiesis of myelodysplastic syndrome. Experimental hematology 23 10029161
1993 Erythropoietin receptor (EpoR)-dependent mitogenicity of spleen focus-forming virus correlates with viral pathogenicity and processing of env protein but not with formation of gp52-EpoR complexes in the endoplasmic reticulum. Journal of virology 23 8437218
2022 Amplified EPOR/JAK2 Genes Define a Unique Subtype of Acute Erythroid Leukemia. Blood cancer discovery 22 35839275
2019 Aqueous extract from You-Gui-Yin ameliorates cognitive impairment of chronic renal failure mice through targeting hippocampal CaMKIIα/CREB/BDNF and EPO/EPOR pathways. Journal of ethnopharmacology 22 31055001
1993 Anti-erythropoietin receptor (EPO-R) monoclonal antibodies inhibit erythropoietin binding and neutralize bioactivity. Blood 22 7686789
2013 Erythropoietin receptor (EpoR) agonism is used to treat a wide range of disease. Molecular medicine (Cambridge, Mass.) 21 23615965
2003 Up-regulation of SLAP in FLI-1-transformed erythroblasts interferes with EpoR signaling. Blood 19 12946994
1997 An erythroid and megakaryocytic common precursor cell line (B1647) expressing both c-mpl and erythropoietin receptor (Epo-R) proliferates and modifies globin chain synthesis in response to megakaryocyte growth and development factor (MGDF) but not to erythropoietin (Epo). British journal of haematology 19 9332307
2007 De novo erythropoietin receptor (EPO-R) expression in human neoplastic glial cells decreases with grade of malignancy but is favourably associated with patient survival. Neuropathology and applied neurobiology 18 17493011
2002 Quantitation of the mRNA levels of Epo and EpoR in various tissues in the ovine fetus. Molecular and cellular endocrinology 18 11911958
2012 Dynamic ligand modulation of EPO receptor pools, and dysregulation by polycythemia-associated EPOR alleles. PloS one 17 22253704
1995 Constitutive expression of GATA-1, EPOR, alpha-globin, and gamma-globin genes in myeloid clonogenic cells from juvenile chronic myelocytic leukemia. Blood 17 7795240
2018 Erythropoietin and long-acting erythropoiesis stimulating agent ameliorate non-alcoholic fatty liver disease by increasing lipolysis and decreasing lipogenesis via EPOR/STAT pathway. Biochemical and biophysical research communications 16 30583863
2014 Phenotyping of human melanoma cells reveals a unique composition of receptor targets and a subpopulation co-expressing ErbB4, EPO-R and NGF-R. PloS one 16 24489649
2012 Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. PloS one 16 22808010
2007 STAT3, HIF-1alpha, EPO and EPOR - signaling proteins in human primary ductal breast cancers. Folia histochemica et cytobiologica 16 17597020
2016 Expression of Hypoxia-Inducible Factor 1α in Invasive Breast Cancer with Metastasis to Lymph Nodes: Correlation with Steroid Receptors, HER2 and EPO-R. Advances in clinical and experimental medicine : official organ Wroclaw Medical University 15 27629849
2015 Functional EpoR pathway utilization is not detected in primary tumor cells isolated from human breast, non-small cell lung, colorectal, and ovarian tumor tissues. PloS one 15 25807104
2018 The Effects of Curcumae Longae Radix, Curcuma phaeocaulis Radix and Their Processed Products on Epo/EpoR Pathway and CD62p. Frontiers in pharmacology 14 30038572
2014 Polycythaemia-inducing mutations in the erythropoietin receptor (EPOR): mechanism and function as elucidated by epidermal growth factor receptor-EPOR chimeras. British journal of haematology 14 24533580
2016 Tumor biology of non-metastatic stages of clear cell renal cell carcinoma; overexpression of stearoyl desaturase-1, EPO/EPO-R system and hypoxia-related proteins. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 13 27468719
2013 The relationships between hypoxia-dependent markers: HIF-1alpha, EPO and EPOR in colorectal cancer. Folia histochemica et cytobiologica 13 24497137
2009 STAT3 and hypoxia induced proteins--HIF-1alpha, EPO and EPOR in relation with Bax and Bcl-xL in nodal metastases of ductal breast cancers. Folia histochemica et cytobiologica 13 20164027
2024 Erythropoietin regulates energy metabolism through EPO-EpoR-RUNX1 axis. Nature communications 12 39284834
2021 Erythropoietin Protects against Diffuse Alveolar Hemorrhage in Mice by Regulating Macrophage Polarization through the EPOR/JAK2/STAT3 Axis. Journal of immunology (Baltimore, Md. : 1950) 12 33811103
2019 EPO-R+ myelodysplastic cells with ring sideroblasts produce high erythroferrone levels to reduce hepcidin expression in hepatic cells. Blood cells, molecules & diseases 12 31082798
2014 Activity increase in EpoR and Epo expression by intranasal recombinant human erythropoietin (rhEpo) administration in ischemic hippocampi of adult rats. Neuroscience letters 12 25219375
2013 B acute lymphoblastic leukemia with t(14;19)(q32;p13.1) involving IGH/EPOR: a clinically aggressive subset of disease. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 12 24030742
2009 Total saponins of Panax ginseng (TSPG) promote erythroid differentiation of human CD34+ cells via EpoR-mediated JAK2/STAT5 signaling pathway. Journal of ethnopharmacology 12 19735711
2023 RNA N6-methyladenosine reader IGF2BP3 promotes acute myeloid leukemia progression by controlling stabilization of EPOR mRNA. PeerJ 11 37663284
2022 Erythropoietin Receptor (EPOR) Signaling in the Osteoclast Lineage Contributes to EPO-Induced Bone Loss in Mice. International journal of molecular sciences 11 36233351
2020 Phospho-PTM proteomic discovery of novel EPO- modulated kinases and phosphatases, including PTPN18 as a positive regulator of EPOR/JAK2 Signaling. Cellular signalling 11 32027948
2018 A truncating mutation in EPOR leads to hypo-responsiveness to erythropoietin with normal haemoglobin. Communications biology 11 30271932
2017 Activation of the EPOR-β common receptor complex by cibinetide ameliorates impaired wound healing in mice with genetic diabetes. Biochimica et biophysica acta. Molecular basis of disease 11 29223734
2015 EPOR-Based Purification and Analysis of Erythropoietin Mimetic Peptides from Human Urine by Cys-Specific Cleavage and LC/MS/MS. Journal of the American Society for Mass Spectrometry 11 26122516
2012 Spry1 as a novel regulator of erythropoiesis, EPO/EPOR target, and suppressor of JAK2. Blood 11 22508938
2010 Immunohistochemical detection of phosphorylated JAK-2 and STAT-5 proteins and correlation with erythropoietin receptor (EpoR) expression status in human brain tumors. Journal of neuro-oncology 11 20336349
2020 Novel mutations in the EPO-R, VHL and EPAS1 genes in the Congenital Erythrocytosis patients. Blood cells, molecules & diseases 10 32739800
2020 Identification and Functional Analysis of EPOR+ Tumor-Associated Macrophages in Human Osteosarcoma Lung Metastasis. Journal of immunology research 10 32908942
2016 Phosphorylated CIS suppresses the Epo or JAK2 V617F mutant-triggered cell proliferation through binding to EpoR. Cellular signalling 10 28038963
2003 Hematopoietic cell survival signals are elicited through non-tyrosine-containing sequences in the membrane-proximal region of the erythropoietin receptor (EPOR) by a Stat5-dependent pathway. Experimental hematology 10 14662339
2008 KIT associated intracellular tyrosines play an essential role in EpoR co-signaling. Cellular signalling 9 18538998
2022 An inherited gain-of-function risk allele in EPOR predisposes to familial JAK2V617F myeloproliferative neoplasms. British journal of haematology 8 35355248
2018 A case of primary familial congenital polycythemia with a novel EPOR mutation: possible spontaneous remission/alleviation by menstrual bleeding. International journal of hematology 7 29623657
2017 EPOR2/βcR2-independendent effects of low-dose epoetin-α in porcine liver transplantation. Bioscience reports 7 29127105
2012 The expression of EPOR in renal cortex during postnatal development. PloS one 7 22844537
2013 Changes in the Expression of Transcription Factors Involved in Modulating the Expression of EPO-R in Activated Human CD4-Positive Lymphocytes. PloS one 6 23577103
2011 Mast cells in canine mammary gland tumour: number, distribution and EPOR positivity. Veterinary and comparative oncology 6 22077413
2000 SPI-1 transforming properties depend upon specifically activated forms of the EPOR. Oncogene 6 11042699
2025 Overview of preclinical and phase II clinical studies on Pegmolesatide's long-term erythropoiesis stimulating effect via EPOR-mediated signal transduction. Journal of translational medicine 5 39894850
2023 EPOR activation attenuates colitis via enhancing LC3B-dependent apoptotic cell clearance. Immunology 5 37204242
2023 EpoR Activation Stimulates Erythroid Precursor Proliferation by Inducing Phosphorylation of Tyrosine-88 of the CDK-Inhibitor p27Kip1. Cells 5 37443738
2017 Do All X-ray Structures of Protein-Ligand Complexes Represent Functional States? EPOR, a Case Study. Biophysical journal 5 28256220
2009 Relationships of P53 and Bak with EPO and EPOR in human colorectal cancer. Anticancer research 5 19846965
2006 Growth control of hybridoma cells with an artificially induced EpoR-gp130 heterodimer. Cytotechnology 5 19002875
2024 Shengmaisan combined with Liuwei Dihuang Decoction alleviates chronic intermittent hypoxia-induced cognitive impairment by activating the EPO/EPOR/JAK2 signaling pathway. Chinese journal of natural medicines 4 38796216
2024 Microglial EPOR Contribute to Sevoflurane-induced Developmental Fine Motor Deficits Through Synaptic Pruning in Mice. Neuroscience bulletin 4 38907076
2022 Identification of Two Novel EPOR Gene Variants in Primary Familial Polycythemia: Case Report and Literature Review. Genes 4 36292571
2015 Mystery Story about Erythropoietin (Epo) and Erythropoietin Receptor (EpoR) are Disguised? Hepato-gastroenterology 4 26897933
2006 Immunohistochemical expression of p53, Bcl-2, COX-2, C-erb-B2, EPO-R, beta-catenin, and E-cadherin in non tumoral gastric mucous membrane. European journal of histochemistry : EJH 4 17213037
2022 Erythroid-specific inactivation of Slc12a6/Kcc3 by EpoR promoter-driven Cre expression reduces K-Cl cotransport activity in mouse erythrocytes. Physiological reports 3 35274823
2016 Development of acute lymphoblastic leukemia with IgH-EPOR in a patient with secondary erythrocytosis. International journal of hematology 3 27544511
2011 [EPOR and TPOR expressions on CD34+ CD59- and CD34+ CD59+ bone marrow cells from patients with paroxysmal nocturnal hemoglobinuria]. Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 3 22338178
2024 Angiogenic responses are enhanced by recombinant human erythropoietin in a model of periventricular white matter damage of neonatal rats through EPOR-ERK1 signaling. Journal of neuropathology and experimental neurology 2 38263262
2023 Learning induces EPO/EPOr expression in memory relevant brain areas, whereas exogenously applied EPO promotes remote memory consolidation. Synapse (New York, N.Y.) 2 37794768
2022 Novel mutations in EPO-R and oxygen-dependent degradation (ODD) domain of EPAS1 genes-a causative reason for Congenital Erythrocytosis. European journal of medical genetics 2 35395428
2008 EPO-R expression patterns in resected gastric adenocarcinoma followed by adjuvant chemoradiation treatment. Pathology oncology research : POR 2 19002606

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